A new role for P2 receptors: talking with calcium-activated potassium channels Bertrand, P. P en_US 2021-11-25T13:34:27Z 2021-11-25T13:34:27Z 2007 en_US
dc.description.abstract Abstract Purinergic fast synaptic transmission may play a very subtle role in regulating the excitability of enteric circuits. That is one of the important findings in a new paper by Ren and Galligan in the current issue of this Journal. They first provide compelling evidence that P2X3 receptors (ionotropic purine receptors) are expressed by guinea-pig motor and interneurons and that these subtypes mediate the purinergic fast excitatory postsynaptic potential (EPSP). They also found that the P2X3-mediated depolarization was often followed by a hyperpolarization. This is an intriguing finding because if the purinergic fast EPSPs are also followed by a hyperpolarization, then it could play a role in truncating bursts of synaptic potentials or in shaping periodic synaptic input. The hyperpolarization is caused by calcium entry through the P2X3 receptor which then activates a calcium-activated potassium (KCa) channel. Surprisingly, the hyperpolarization was not affected by any of the standard blockers of calcium- or voltage-activated K+ channels suggesting that a novel KCa channel is present in the enteric neurons. Such a wide-spread channel could well have an important physiological role and could be an important new drug target for regulating reflex activity in the enteric nervous system en_US
dc.identifier.issn 1350-1925 en_US
dc.language English
dc.language.iso EN en_US
dc.rights CC BY-NC-ND 3.0 en_US
dc.rights.uri en_US
dc.source Legacy MARC en_US
dc.title A new role for P2 receptors: talking with calcium-activated potassium channels en_US
dc.type Journal Article en
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dspace.entity.type Publication en_US
unsw.identifier.doiPublisher en_US
unsw.relation.faculty Medicine & Health
unsw.relation.ispartofissue 11 en_US
unsw.relation.ispartofjournal Neurogastroenterology & Motility en_US
unsw.relation.ispartofpagefrompageto 865-868 en_US
unsw.relation.ispartofvolume 19 en_US
unsw.relation.originalPublicationAffiliation Bertrand, P. P, Medical Sciences, Faculty of Medicine, UNSW en_US School of Medical Sciences *
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